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Clinical findings and treatment of 30 cattle with botulism.

The clinical signs, the results of haematological and biochemical analyses and the treatment of 30 cattle with botulism are described, and the signs of the 13 cattle that survived are compared with those of the 17 that were euthanased owing to the disease. The cattle originated from 11 farms that had experienced an outbreak of botulism. The most important clinical sign in all the cattle was a reduction in the strength of the tongue; excessive salivation and difficulty in swallowing were observed in 20 of the animals, and the ears of 15 of them drooped. In 21 of the cattle, reaction to pricking of the head and body with a hypodermic needle was either absent or slight. Twelve of the animals had an unsteady, slow, difficult gait, and nine were unable to stand. A significantly higher proportion of the cattle which were euthanased had marked changes in behaviour and condition, anorexia, severely reduced skin turgor, weak tongues, a low rectal temperature, a high heart rate and a low blood pH; 11 were euthanased immediately after a clinical examination and six were euthanased one to five days after the initiation of treatment because their condition had deteriorated. Thirteen of the animals were treated for three to 23 days and were healthy when they were discharged. The treatment consisted of an intravenous infusion of 10 to 20 litres of glucose saline per day and the daily administration of fresh ruminal juice. Follow-up by telephone several months later revealed that all 13 animals had recovered completely.

Animals↗

A comparison of human and animal botulism: a review.

Botulism can arise from preformed toxin, wound infection or intestinal toxico-infection. All three forms can occur in humans as well as in animals. The examination of botulism in veterinary practice can alert the medical profession to the hazards which can occur with the introduction of dietary alterations and hermetic sealing of foodstuffs. There is also the possibility that the development of pica through lack of essential nutrients could lead to the ingestion of contaminated substances rendering the child (or even adult) susceptible to botulinum intoxication. A positive gain has been that research leading to the elimination of shaker foal disease has provided a comprehensive analysis of factors which may underline the risk of toxico-infection in infants.

Animals↗

Severe adult botulism.

A case of severe adult botulism with paralysis, respiratory failure and cranial nerve palsies is presented. The pathophysiology, clinical manifestations, diagnosis and treatment options for botulism are discussed.

Botulinum Toxins↗

Type C botulism in turkeys: determination of the median toxic dose.

The median toxic dose (TD50) of type C botulinum in turkeys was determined using an up-and-down method for toxicologic testing. Birds were dosed intravenously with 10, 20, or 40 mouse lethal dose per kilogram body weight (MLD/kg) of type C botulism toxin and observed for 5 days. Administration of toxin resulted in acute death, posterior paresis, or no effect, depending upon the dose. The TD50 causing posterior paresis was calculated as 25.75 MLD/kg (confidence interval = 17.08-38.82 MLD/kg). Posterior paresis was identified as the principal sign associated with sublethal botulism toxicosis in turkeys. The resultant posterior paresis was similar to the clinical syndrome observed in an unsolved field investigation.

Aging↗

Management of botulism.

OBJECTIVE: To provide a concise review of the presentation and treatment of botulism. DATA SOURCES: Searches of MEDLINE (1966-November 2001), tertiary references, and public and government Internet sites were conducted. STUDY SELECTION: All articles and additional references from those articles were thoroughly evaluated. DATA SYNTHESIS: Clostridium botulinum toxin blocks acetylcholine release in a dose-dependent fashion, resulting in acute symmetric diplopia, dysarthria, dysphonia, dysphagia, and possible neurologic sequelae despite the route of exposure (i.e., food-borne, wound, intestinal, inhalation). Disease secondary to genetically engineered C. botulinum may differ from that of inadvertent exposure. Present treatment is primarily supportive care, respiratory support, rapid decontamination, and antitoxin administration (i.e., trivalent, pentavalent, heptavalent antitoxin). Early initiation of antitoxin limits the extent of paralysis, but does not reverse it. CONCLUSIONS: Supportive care and the use of antitoxin have been effective in the treatment of botulism from food-borne, intestinal, and wound exposure. However, the effectiveness of antitoxin in the treatment of inhaled C. botulinum has not been proven.

Antitoxins↗

Association between honey consumption and infant botulism.

Infant botulism, a disease that results in a blockade of voluntary motor and autonomic functions, was first recognized in the United States in the late 1970s. Since then, more than 1000 cases in this country have been reported to the Centers for Disease Control and Prevention (CDC). Numerous studies have shown that the ingestion of honey is linked with infant botulism. In addition, honey samples across the United States have tested positive for Clostridium botulinum spores and toxins. Such substantial evidence led the CDC to recommend that honey not be given to infants younger than 12 months old. It is important that clinicians be familiar with this risk and should not recommend honey-containing products or supplements or the use of honey as a flavoring agent for infants in this age group.

Botulism↗

Garlic-in-oil associated botulism: episode leads to product modification.

In February 1989, three cases of botulism occurred in persons who consumed garlic bread made from a garlic-in-oil product. Testing of leftover garlic-in-oil showed it to have a pH of 5.7 and to contain high concentrations of Clostridium botulinum organisms and toxin. This was the second episode of botulism associated with a low acid garlic-in-oil product which needs constant refrigeration. In response, the Food and Drug Administration has taken steps to prevent a recurrence by requiring that microbial inhibitors or acidifying agents be added to such products.

Adult↗

Biological agents as weapons 1: smallpox and botulism.

1. Early recognition by clinicians of illnesses suggesting a biological attack is integral to the public health response. 2. The four biological agents of most concern are smallpox virus, botulinum toxin, and anthrax and plague bacteria. 3. Smallpox is distinguishable from chickenpox by the prominent prodromal period and lesions that develop at the same pace and, on any part of the body, appear identical to each other, evolve slowly and are peripherally distributed. 4. The degree of protection conferred by smallpox vaccination given 20 or more years ago is unknown. 5. Foodborne and inhalational botulism could result from deliberate release of toxin. 6. Botulism presents with cranial nerve palsies and descending paralysis in a patient with normal conscious state and no fever.

Bioterrorism↗

Clinical features of types A and B food-borne botulism.

Medical records of 55 patients with type A and type B food-borne botulism reported to the Centers for Disease Control during 2 years were reviewed to assess the clinical features and severity of illness, diagnostic test results, nature of complications, amd causes of death. Some patients had features not usually associated with botulism including paresthesia (14%), asymmetric extremely weakness (17%), asymmetric ptosis (8%), slightly elevated cerebrospinal fluid protein values (14%), and positive responses to edrophonium chloride(26%). Several observation suggest that type A was more severe than type B disease. Although the case-fatality ratio was not significantly greater, patients with type A disease saw a physician earlier in the course of illness, were more likely to need ventilatory support, and were hospitalized longer. Patients who died were older than those who survived. Deaths within the first 2 weeks resulted from failure to recognized the severity of the disease or from pulmonary or systemic infection whereas the three late deaths were related to respirator malfunction.

Adult↗

A relationship between avian carcasses and living invertebrates in the epizootiology of avian botulism.

A survey of the sources of Clostridium botulinum type C toxin possibly utilized as food by aquatic birds in an epizootic area of avian botulism in northern Utah showed that living aquatic and terrestrial invertebrates normally found in close association with dead, decomposing birds commonly carried the toxin. Of 461 samples associated with 21 species of avian carcasses, 198 were toxin-positive. Invertebrate species not normally scavengers of vertebrate tissues were less commonly and less highly toxic, particularly when captured 30 cm or more from a carcass; six of 237 samples of such aquatic invertebrates low-level toxin. Of the species tested, blow fly larvae (Calliphoridae) were the most consistently and highly toxic, although others, particularly adult and larval stages of several species of beetles (Coleoptera), contained toxin at levels probably significant in the epizootiology of the disease. An estimated 0.05 to 0.25 g of the most toxic fly larvae or 15 g of the most toxic beetles tested carried a mediam lethal dose for an adult mallard duck. Examination of stomach contents of aquatic birds dead of botulism showed that some had consumed invertebrates.

Animals↗

An epizootic of avian botulism in a phosphate mine settling pond in northern Florida.

Type C botulism was determined to be the cause of an epizootic among waterfowl and shorebirds in a phosphate mine settling pond in northern Florida during May and June of 1979. Several hundred birds, the most common of which were American coots (Fulica americana), wood ducks (Aix sponsa), common gallinules (Gallinula chloropus), and northern shovelers (Anas clypeata), were afflicted over about a three-week period. A second smaller outbreak occurred in the same pond in early December of 1979. This is apparently the first time that botulism has been reported in waterbirds of Florida.

Animals↗

Effects of botulism on ducks drinking saline water.

Mallard (Anas platyrhynchos) ducklings (2 wk old) were given water from natural saline wetlands or fresh water as drinking water for 1 or 2 wk prior to, and after, receiving material containing Clostridium botulinum type C toxin. Water with conductivity ranging from 3,460 to 6,690 mu mhos/cm had no detectable effect on the occurrence or severity of clinical signs of botulism. Ducks drinking water with conductivity of 7,130 mu mhos/cm for 1 wk prior to receiving toxin had more severe clinical signs and greater mortality than did birds drinking fresh water. Ducks given the same water for 2 wk prior to receiving toxin did not differ from the controls in response to toxin. Fewer ducks in groups drinking the most saline water tested (conductivity = 13,500 mu mhos/cm) had clinical signs of botulism than in groups drinking fresh water.

Animals↗

An outbreak of type E botulism among common loons (Gavia immer) in Michigan's upper peninsula.

An epizootic of type E botulism (Clostridium botulinum) occurred among common loons (Gavia immer) along the Lake Michigan shore of Michigan's Upper Peninsula (USA) during October and November 1983. An estimated 592 dead loons washed ashore along the Garden Peninsula. Type E botulinal toxin was demonstrated in blood samples and stomach contents of dead loons, and in samples of three species of dead fish found on the Lake Michigan shore. We suspect that loons acquired botulism by ingesting sick or dead fish containing type E toxin.

Animals↗

Brain acetylcholinesterase activity in botulism-intoxicated mallards.

Brain acetylcholinesterase (AChE) activity in captive-reared mallards (Anas platyrhynchos) that died of botulism was compared with euthanized controls. AChE levels for both groups were within the range reported for normal mallards, and there was no significant difference in mean AChE activity between birds that ingested botulism toxin and died and those that did not.

Acetylcholinesterase↗

Immunization of ducks for type C botulism.

A single subcutaneous immunization with a vaccine used for protecting ranch mink (Mustela vison) against type C botulism reduced morbidity and mortality in mallard (Anas platyrhynchos) and northern pintail (Anas acuta) ducks challenged with approximately 4.5 x 10(4) and 2.25 x 10(4) mouse lethal doses (MLD50), respectively, of botulinum toxin at 10 and 15 days post-immunization (pi). There was no significant protection at 5 days pi. Protection persisted in mallards for 90 days pi. To simulate use of vaccine as a part of treatment of sick birds in the field, mallards were exposed to toxin and, when clinical signs were evident, each bird was treated by intraperitoneal injection of type C botulinum antitoxin and one-half of the birds were immunized. Immunization had no significant effect on recovery from intoxication. At 10 days posttreatment, all birds were challenged with toxin. Clinical signs and mortality were significantly less frequent among immunized birds than among non-immunized birds after the second exposure. Immunization might be useful as part of the treatment regimen in botulism outbreaks.

Animals↗

Toxicity of Clostridium botulinum type E neurotoxin to Great Lakes fish: implications for avian botulism.

Since 1999, large-scale mortalities of fish-eating birds have been observed on the Great Lakes, and more specifically on Lake Erie. Type E botulism has been established as the primary cause of death. The mechanism of type E botulism exposure in fish-eating birds is unclear. Given that these birds are thought to eat live fish exclusively, it seems likely that their prey play a key role in the process, but the role of fish as potential transport vectors of botulinum neurotoxin type E (BoNT/E) to birds has not been adequately investigated. Between June 2003 and April 2004 a methodological model for exposing fish to Clostridium botulinum was developed and used to compare the sensitivity of rainbow trout (Oncorhynchus mykiss), round goby (Neogobius melanostomas), walleye (Stizostedion vitreum), and yellow perch (Perca flavescens) to four doses (0, 800, 1,500, and 4,000 Mouse Lethal Doses) of Clostridium botulinum type E neurotoxin. Each fish species expressed unique changes in both behavior and skin pigmentation prior to death. Yellow perch survived significantly longer (P < 0.05) than the three other species at all toxin treatments. Results of this study suggest that live fish can represent a significant vector for transfer of BoNT/E to birds.

Animals↗

Foodborne botulism associated with home-canned bamboo shoots--Thailand, 1998.

On April 13, 1998, the Field Epidemiology Training Program in the Thailand Ministry of Public Health (TMPH) was informed of six persons with sudden onset of cranial nerve palsies suggestive of botulism who were admitted to a provincial hospital in northern Thailand. To determine the cause of the cluster, TMPH initiated an investigation on April 14. This report summarizes the results of the investigation, which indicate that the outbreak was caused by foodborne botulism from home-canned bamboo shoots.

Adult↗